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Tianyan Gao

Researcher at University of Kentucky

Publications -  102
Citations -  7853

Tianyan Gao is an academic researcher from University of Kentucky. The author has contributed to research in topics: Protein kinase B & Phosphorylation. The author has an hindex of 40, co-authored 94 publications receiving 6934 citations. Previous affiliations of Tianyan Gao include University of California, San Diego & Northwestern University.

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PHLPP: A Phosphatase that Directly Dephosphorylates Akt, Promotes Apoptosis, and Suppresses Tumor Growth

TL;DR: PHLPP levels are markedly reduced in several colon cancer and glioblastoma cell lines that have elevated Akt phosphorylation, consistent with PHLPP terminating Akt signaling by directly dephosphorylating and inactivating Akt.
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PHLPP and a Second Isoform, PHLPP2, Differentially Attenuate the Amplitude of Akt Signaling by Regulating Distinct Akt Isoforms

TL;DR: The data unveil a mechanism to selectively terminate Akt-signaling pathways through the differential inactivation of specific Akt isoforms by specific PHLPP isoforms.
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Na/K-ATPase Y260 Phosphorylation-mediated Src Regulation in Control of Aerobic Glycolysis and Tumor Growth

TL;DR: The discovery of Y260 in α1 Na/K-ATPase as a Src-specific phosphorylation and binding site is discovered and it is suggested that the role of this regulation in control of Warburg effect and tumor growth may lead to Warburg phenotype in cancer.
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cAMP-Dependent Regulation of Cardiac L-Type Ca2+ Channels Requires Membrane Targeting of PKA and Phosphorylation of Channel Subunits

TL;DR: The PKA-mediated regulation of L-type Ca2+ channels is critically dependent on a functional AKAP and phosphorylation of the alpha1C subunit at Ser1928, demonstrating that the events observed in the heterologous expression system reflect those occurring in the native system.
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mTORC1 and mTORC2 regulate EMT, motility and metastasis of colorectal cancer via RhoA and Rac1 signaling pathways

TL;DR: It is found that increased expression of mTOR, Raptor, and Rictor mRNA was noted with advanced stages of CRC, suggesting that mTOR signaling may be associated with CRC progression and metastasis, and provides the rationale for including mTOR kinase inhibitors, which inhibit both mTORC1 and m TORC2, as part of the therapeutic regimen for CRC patients.